Three equine herpesviruses (EHV-1,2,3) that differ in biological and biochemical properties will be studied. EHV-1 causes systemic infection that may be abortigenic; EHV-2 is a cytomegalovirus associated with several diseases; EHV-3 causes a venereal disease. They offer ideal models in animals (in vivo) and cell cultures to study biochemical and biological activities of herpesvirus infection: EHV-infected hamsters and cell cultures allow study of the biochemistry of cytocidal infection and purification of particles and products for characterizing viral molecular anatomy and viral macromolecules. Serial, high multiplicity EHV-1 passage in animals and LM cells yields different populations of defective interering (DI) particles (that vary in biological activities and genetic complexity) for study of altered virus replication. These DI particles persistently infect LM cells and oncogenically transform LSH hamster cell (unpublished). Also, UV-inactivated EHV-1 transforms permissive LSH cells, and viral DNA (transfection) transforms nonpermissive BALB/c mouse cells. These cells harbor viral DNA sequences (unpublished) and produce transplantable sarcomas. Continued research concerns: I. Elucidation and comparison of the structure of the genomes of these three related herpesviruses by restriction enzyme mapping techniques. DNA-DNA hybridization analyses of the genomes and fragments will measure the exact genetic relatedness (less than 10%) and identify the isolation of shared sequences. Also, the viral DNAs of DI particles will be mapped. II. Key biological and biochemical properties of the cytomegalovirus will be compared to those already revealed for EHV-1, such as structure (enzyme mapping) and biophysical properties (S value, M. WT, etc.) of the DNA, virion polypeptides (gel electrophoresis), properties of viral DNA polymerase, effect of infection on cellular DNA replication, etc. III. The oncogenic potential of EHV-2 and -3 will be tested. EHV-1, 2, and 3 transformed and tumor LSH cells will be compared for: 1) tumor dose, pathology, karyotype, etc., 2) viral particles and enzymes by specific assays, 3) presence and amount of viral DNA by hybridization with 125I EHV DNAs and fragments, and 4) identification of viral proteins by immunofluorescence, immunoprecipitation, etc. D (Text Truncated -Exceeds Capacity)